Case study: I am 25 years old. 14 years old with hepatitis B onset transaminase 254 U/L, recovered to 30 U/L after 10 days of liver care to lower the enzyme. The results of a high-sensitivity accurate test six months ago were 180 IU/ml. 2988 IU/ml of surface antigen. methemoglobin was checked three times in the last year, once at 9.1 and twice at 7.5 (threshold 8.8ng). ultrasound showed no abnormalities. The questions are as follows: 1. My father died of liver cancer at the age of 34. With this family history, do I need to consider antiviral treatment now? If not, what phenomenon occurs that requires it? 2. How much does family history affect? Reading your blog, I learned that liver cancer has a genetic predisposition. If I keep this test result and take care of my life, what is the probability of getting liver cancer? Is it much higher than normal people? 3. I was found to have elevated transaminases during an accidental physical examination at the age of 14 and developed the disease, does the age of onset have any effect on the development of the disease in the future? My father has liver cancer and I have chronic hepatitis B virus infection, so of course I must be alert. With the hereditary quality of liver cancer, there also needs to be a basis for receiving the hereditary lesion. With chronic hepatitis B virus infection, one must also look at the liver lesions, the more severe the lesions, the higher the incidence. According to the existing test results, it is only chronic inactive carriage and there should be no need to worry. The problem is: 11 years since the onset of hepatitis at the age of 14, the first 7 years did not check the liver function; the virus has been checked 5 times negative in recent years, recently the precise quantitative virus positive, it is difficult to determine whether there has been disease activity. It is difficult to determine whether there has been any liver fibrosis because the lesions of “minor triplets” can potentially develop without regular checkups in the past. Cirrhosis and chronic hepatitis fibrosis are the underlying lesions for the development of liver cancer. It is recommended to do liver fibrosis scan, blood work, liver function including GGT, and methemoglobin, and consider CT scan if there is any abnormality. The virus that increases in “small triplet” is mutated and less virulent, and transaminases can be normal in a few hepatitis patients, so the virus level is more important for diagnosis. The current baseline is a precise quantification of 5 times cp/ml, to which weights must be added. The threshold for diagnosis can also be lowered if severe liver fibrosis is present. With the exclusion of liver fibrosis, there is no need to worry, except that chronic inactive carriage of the virus and lesions may become active again, as long as liver function, viral, ultrasound and methemoglobin are checked every 6 months thereafter is the best guarantee of safety. Liver function and viral quantification can monitor hepatitis; once the disease develops, ultrasound and methotrexate can monitor cancer, and small liver cancer can be eradicated within 6 months.